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PubMed1997

[Treatment of post-herpes zoster pain with tramadol. Results of an open pilot study versus clomipramine with or without levomepromazine].

To date, no universally applicable recommendations are available for the treatment of patients with postherpetic neuralgia. A mixture of clinical anecdotes, experimental findings and observations from clinical trials form the basis of the medical arsenal for this condition. Tricyclic antidepressants are commonly used, and clinical experience and several investigations have documented their effectiveness. Today, single entity antidepressants, which can be combined with neuroleptics to increase analgesia, are generally recommended for the treatment of postherpetic neuralgia. Some authors also recommend the additional administration of an opioid if analgesia is inadequate. Just over a decade ago, opioids were considered ineffective for the treatment of neuropathic pain; however, more recent investigations relating to the use of opioids, primarily in the treatment of nontumour-related chronic pain, have led to a revision of their use in neuropathic pain. Nevertheless, the use of opioid therapy for neurogenic pain remains controversial. Tramadol is a synthetic, centrally acting analgesic with both opioid and nonopioid analgesic activity. The nonopioid component is related to the inhibition of noradrenaline (norepinephrine) reuptake and stimulation of serotonin (5-hydroxytryptamine; 5-HT) release at the spinal level. In this regard, there are parallels with antidepressants, which are believed to potentiate the effect of biogenic amines in endogenous pain-relieving systems. There is evidence that, in tramadol, both mechanisms act synergistically with respect to analgesia. The aim of this pilot study was to investigate, for the first time, the analgesic efficacy and tolerability of tramadol, compared with the antidepressant clomipramine, in the treatment of postherpetic neuralgia. If necessary, clomipramine was used in combination with the neuroleptic levomepromazine. The study allowed individualised dosages at predetermined intervals up to a maximum daily dose of tramadol 600mg and clomipramine 100mg, or clomipramine 100mg with or without levomepromazine 100mg. 21 (60%) of 35 randomised patients (> or = 65 years) received the study medication over the 6-week period [tramadol n = 10; clomipramine with or without levomepromazine) n = 11]. After 3 weeks' treatment the dosage in both groups remained almost constant for the rest of the 6-week treatment phase (mean daily dose: tramadol 250 to 290mg; clomipramine 59.1 to 63.6mg). Only 3 patients required the combination of clomipramine and levomepromazine. At the outset, both groups recorded an average pain level of 'moderate' to 'very severe'. In correlation with increasing the study medication, this had decreased to 'slight' by the end of the treatment, when 9 of 10 patients in the tramadol group and of 6 of 11 patients in the clomipramine group retrospectively rated their analgesia as excellent, good or satisfactory. The psychological/physical condition of the patients did not change significantly during tramadol treatment. Sensitivity and depression parameters decreased in the clomipramine group. The incidence of adverse events for all patients was similar in both groups (tramadol 76.5%; clomipramine with or without levomepromazine 83.3%). In conclusion, tramadol would appear to be an interesting therapeutic alternative for pain relief in postherpetic neuralgia, particularly in patients who are not depressed. In clinical practice, tramadol and clomipramine can best be used differentially. For example, tramadol could be the drug of first choice in patients with obvious cardiovascular disease (not an uncommon problem in the > or = 65 year age group) in whom antidepressants are contraindicated, and similarly in patients in whom an antidepressant effect is not required. (ABSTRACT TRUNCATED)

Aged↗
PubMedDate not supplied

High performance liquid chromatographic determination of levomepromazine in human breast milk and serum using solid phase extraction.

A high performance liquid chromatographic (HPLC) method has been developed for the determination of levomepromazine in human breast milk and serum. The levomepromazine was extracted by a rapid and simple extraction method using a Sep-Pak C18 cartridge. The extracts were separated by HPLC on a C8 bonded reversed phase column and detected by UV absorbance at 254 nm. There was no interference with endogenous substance in human breast milk and serum. A linear relationship was obtained for the levomepromazine over the concentration range of 10-300 ng/mL. The recoveries of levomepromazine added to human breast milk and serum were 92.5-99.1% and 86.9-103.9%, respectively.

Chromatography, High Pressure Liquid↗
PubMed1997

Increased plasma concentrations of bromperidol and its reduced metabolite with levomepromazine, but not with thioridazine.

Bromperidol is a close structural analog of haloperidol. The authors studied the effects of levomepromazine and thioridazine, which are frequently added to other neuroleptics as sedatives, on plasma concentrations of bromperidol and its reduced metabolite. The subjects were 26 inpatients with schizophrenia receiving bromperidol, 12 to 24 mg/day, for 1 to 19 weeks. In 10 cases, 50 mg levomepromazine per day and in nine cases, 50 mg thioridazine per day were coadministered for 1 week. In seven cases, both drugs were coadministered with > or = 2-week intervals. Plasma concentrations of bromperidol and reduced bromperidol were measured by a high-performance liquid chromatographic method. Levomepromazine (n = 17) significantly (p < 0.001) increased plasma concentrations of bromperidol (7.3 +/- 4.1 versus 10.2 +/- 4.8 ng/ml) and reduced bromperidol (1.8 +/- 1.4 versus 4.5 +/- 3.3 ng/ml). Thioridazine (n = 16) did not significantly change plasma concentrations of bromperidol (9.1 +/- 5.7 versus 8.6 +/- 5.5 ng/ml), while those of reduced bromperidol could not be measured because of interfering peaks. The current study suggests that levomepromazine, but not thioridazine, increases plasma concentrations of bromperidol and reduced bromperidol by inhibiting the metabolism of these compounds.

Adult↗
PubMed2000

Solid-phase microextraction for the assay of levomepromazine in human plasma.

Solid-phase microextraction (SPME) was investigated as sample preparation for the assay of the neuroleptic drug levomepromazine in human plasma. A mixture of human plasma, water, chloramitriptyline as internal standard, and aqueous NaOH was extracted with a 100-microm polydimethylsiloxane (PDMS) fiber (Supelco). The desorption of the fiber was performed in the injection port of a gas chromatograph at 260 degrees C [HP 5890; BPX-5 (SGE): 30 m x 0.53 mm ID, 1-microm film capillary; nitrogen-phosphorus selective detection]. As repeatedly found for SPME analysis of drugs in plasma, the recovery was low (i.e., 7% for levomepromazine). However, the analyte and internal standard were well separated and the calibration was linear from 5 to 180 ng/mL. The within-day precision was 2%, 4%, and 19% at concentrations of 160 ng/mL, 80 ng/mL, and 5 ng/mL, respectively. The between-day precision was 3%, 7%, and 19%, respectively. The limit of determination was 5 ng/mL. The comparison with an established liquid-liquid extraction gas-liquid chromatography method revealed good agreement for spiked samples and patient samples. No interfering peaks of drugs coadministered with levomepromazine or of endogenous substances were found. It is concluded that the method can be used in the therapeutic drug monitoring and clinical toxicology of levomepromazine.

Antipsychotic Agents↗
PubMed1990

The effects of beta-adrenoceptor antagonists and levomepromazine on the metabolic ratio of debrisoquine.

The in vivo inhibitory effect of five beta-adrenoceptor antagonists and levomepromazine on debrisoquine metabolism was assessed in 37 subjects. The debrisoquine phenotyping test was performed before and after 7 days' treatment with oxprenolol (40 mg three times daily), propranolol (20 mg three times daily), timolol (10 mg twice daily), pindolol (5 mg twice daily), metoprolol (50 mg twice daily) or levomepromazine (10 mg daily), each of which was given to six-seven subjects. No clear change in the urinary metabolic ratio of debrisoquine/4-OH-debrisoquine (MR) was seen with any of the single beta-adrenoceptor antagonist treatments, but the MR value increased significantly when all beta-adrenoceptor blocker treatments were considered together. Debrisoquine metabolism was clearly impaired after levomepromazine 10 mg daily for 7 days; the mean MR increased from 1.24 +/- 1.6 to 4.70 +/- 5.23 (P = 0.018) and the excretion of 4-hydroxydebrisoquine decreased from 0.92 +/- 0.46 mg to 0.31 +/- 0.19 mg (P = 0.043). Thus, levomepromazine changes MRs towards those characteristic of phenotypically poor metabolizers, but beta-adrenoceptor antagonists at the doses examined have only a marginal effect.

Adrenergic beta-Antagonists↗
PubMed1964

COMPARATIVE ANALGESIC ACTIVITY OF LEVOMEPROMAZINE AND MORPHINE IN PATIENTS WITH CHRONIC PAIN.

Apart from its ability to potentiate the action of narcotics, levomepromazine, a phenothiazine derivative, was shown to possess its own analgesic activity comparable to that of morphine at a 3:2 dose relationship.In a double-blind crossover study of 18 patients suffering from chronic pain (cancer and arthritis), levomepromazine (15 mg.) was compared with morphine (10 mg.) and placebo. Three hours after intramuscular administration, levomepromazine proved to be significantly superior to placebo (p < .05) and indistinguishable from morphine. Evaluations of pain relief by estimations of changes in pain intensity were found to correlate well with evaluations based on recognition of pain relief exceeding 50%.The potent analgesic effect of levomepromazine was obtained at the price of excessive sedation. This, however, was considered an acceptable side effect in a patient suffering from chronic pain. These results provide encouragement in the quest for a non-addicting substitute for morphine.

Analgesics↗
PubMed2004

[Hair analysis as a document of oxcarbazepine therapy in fatal levomepromazine poisoning].

A development of contemporary analytical methods makes possible to use hairs in toxicological analysis for documentation history of drug administration. An undertaken subject has been illustrated by a suicidal fatal poisoning of 58-year-old man with a neuroleptic drug--levomepromazine. Toxicological analysis carried out by HPLC/APCI/MS, besides of standardized postmortem specimen as blood, urine, liver and cerebrospinal fluid included also victim hairs. As a result of analytical procedure levomepromazine at high concentrations was revealed, which may be responsible for death. Moreover, and antiepileptic drug--oxcarbazepine and two main metabolites at therapeutic concentrations were revealed parallel. In three 2-cm segments of hair oxcarbazepine and two metabolites were detected, levomepromazine, in contrary, was not detected in this specimen. Complex chemical-toxicological investigation confirmed information that victim was an epileptic patient and was treated with oxcarbazepine at least 6 months before death while toxic dose of levomepromazine, as one could suppose, he took to commit suicide.

Anticonvulsants↗
PubMed1977

Pharmacokinetics and relative bioavailability of levomepromazine after repeated administration of tablets and syrup.

Plasma levels of levomepromazine and its sulphoxide were measured in 8 psychiatric patients after repeated doses of levomepromazine tablets or syrup. The rate and extent of absorption of the drug were similar for the two dosage forms, although the extent of presystemic metabolism appeared to be slightly greater after administration of syrup than of tablets. The biological half-life of levomepromazine ranged from 16.5 h to 77.8 h, and a 13-fold variation was seen in the ratio of the total clearance to the absorbed fraction of the dose (Cl/Fpo). It is postulated that individual variation in the dose required for therapy was due in part to individual variation in the pharmacokinetics of the drug.

Administration, Oral↗
PubMed1994

Quantification of chlorprothixene, levomepromazine and promethazine in human serum using high-performance liquid chromatography with coulometric electrochemical detection.

Isocratic reversed-phase high-performance liquid chromatography with coulometric electrochemical detection was optimised to quantify the neuroleptic drugs chloroprothixene, levomepromazine, and promethazine in human serum. The method involves extraction of the neuroleptic drugs in n-heptane-isoamylalcohol from the alkalinized serum, followed by chromatographic separation on a Nucleosil CN column with acetonitrile-pyridine-sodium acetate buffer as the mobile phase. The extraction recovery was > 85% for each neuroleptic drug. The sensitivity and selectivity required for pharmacokinetic studies was obtained with a dual coulometric analytical cell operating in the oxidative screen mode. The lower limit of detection in human serum for chlorprothixene, levomepromazine, and promethazine, was 0.5, 0.2 and 0.1 ng/ml, respectively. A linear relationship (r2 > 0.99) was obtained between the concentrations of each neuroleptic drug and the detector signal. The accuracy of the quality control samples was +/- 7% for each neuroleptic drug with a precision within 9.5%, 8.1% and 13.5% for chlorprothixene, levomepromazine, and promethazine, respectively. The neuroleptic drugs were stable in acetonitrile and human serum for at least six months when stored at -20 degrees C. This method is applicable to analyze a large number of serum samples for pharmacokinetic studies of the neuroleptic drugs.

Chlorprothixene↗
PubMed1982

Simultaneous determination of chlorpromazine and levomepromazine in human plasma and urine by high-performance liquid chromatography using electrochemical detection.

A rapid, selective and sensitive method for the simultaneous determination of chlorpromazine and levomepromazine in human plasma and urine has been developed using high-performance liquid chromatography with electrochemical detection. The unchanged drugs and internal standard extracted from plasma and urine were separated by reversed-phase high-performance liquid chromatography. The influence of acetonitrile concentration and of the pH of the mobile phase were investigated. The detection limits were 100 pg for chlorpromazine and for levomepromazine. In comparison with three other detection systems this was found to be the most sensitive method. This method was successfully applied to the simultaneous determination of chlorpromazine and levomepromazine in human plasma and urine for pharmacokinetic studies.

Chlorpromazine↗
PubMed1999

Death attributed to amobarbital and levomepromazine intoxication.

A 29-year-old man, possibly a schizophrenic patient, was found dead 9 h after admission to a hospital. Autopsy revealed neither significant injuries nor diseases except for congestion of all organs. Microscopic examination revealed severe edema in the lung and slight centrilobular necrosis in the liver. Since amobarbital and levomepromazine were detected by drug screening, the concentrations of these drugs in the victim's body fluids and tissues were determined using gas chromatography-mass spectrometry. The whole blood concentrations of amobarbital and levomepromazine were 9.02 microg/ml and 231 ng/ml, respectively. These levels exceeded therapeutic ranges, but are not so toxic or fatal. However, on the basis of the findings in the literature and of the severe lung edema and centrilobular necrosis in the liver, the cause of his death was judged to be amobarbital and levomepromazine intoxication.

Journal Article↗
PubMed1980

[Improved antiemetic treatment with levomepromazine (author's transl)].

The antiemetic effect of levomepromazine (Neurocil) was tested in 76 patients treated for metastasizing malignancies with cis-dichlorodiammineplatinum (II) (Platinex). In all patients conventional antiemetics had been ineffective against gastrointestinal side effects of platinum. Using levomepromazine vomiting and nausea could be successfully prevented in 47 out of 63 patients on conventional cis-platinum doses (20 mg/m2 for 5 consecutive days) and in 5 out of 13 patients on high single day dosages (100 mg/m2). In most other patients clear-cut subjective improvement occurred. The antiemetic effect of levomepromazine against cis-platinum, which ranks among the most widely used cytostatics and causes gastrointestinal symptoms, is of importance in medico-oncological practice as it causes relief for the patients.

Cisplatin↗
PubMed1982

Effect of levomepromazine on EEG and on clinical side effects after lumbar myelography with metrizamide.

In patients with lumbago-sciatica levomepromazine is a potent supplement to analgetics in pain treatment. The hypothesis that neuroleptics increase the risk of epileptic seizures after metrizamide myelography was not confirmed in a series of 77 patients, 26 with and 51 without levomepromazine medication, before and after lumbar metrizamide myelography. No differences existed between the groups with regard to the appearance of EEG abnormalities such as slow waves or spikes. Mild side effects were more frequent in the levomepromazine group, except nausea and vomiting. Lumbar metrizamide epidurography in 30 patients did not cause any abnormal EEG.

Drug Interactions↗
PubMed2004

Focus on levomepromazine.

This is a review of the uses of levomepromazine in psychiatry, based upon MEDLINE, PSYCLIT and EMBASE literature searches. The main indications for this drug in psychiatry are schizophrenia and schizoaffective disorder. Levomepromazine's sedative properties particularly fit it to use in psychiatric intensive care. There is also some evidence to suggest it has efficacy in drug-resistant psychosis, although this property of the drug does require further research. In other areas of medicine levomepromazine has been used in: alleviating bronchoconstriction; as a preoperative sedative; in terminal pain control and postoperative analgesia; and in the control of nausea. Some antimycobacterial properties have been recorded. The drug should not be prescribed to patients at high risk of accidental or suicidal overdose.

Antipsychotic Agents↗
PubMed2005

Low-dose levomepromazine in refractory emesis in advanced cancer patients: an open-label study.

Seventy patients with advanced cancer and refractory emesis were treated with subcutaneous boluses of levomepromazine (median daily dose: 6.25 mg; range: 3.12-25) in an open-label prospective study. Treatment was associated with a decrease in nausea from a median of 8/10 at baseline (IQR 7-8) to a median of 1 (IQR 0-2) after two days of treatment (P<0.0001); vomiting ceased in 92% of cases. It was possible to remove the nasogastric tube from all 11 patients who had one. The most frequently reported side effect was sedation, with a median of 2/10 (25-75% percentile 1-3), which was not correlated with the dose of levomepromazine. This study suggests that treatment with low-dose levomepromazine is an effective and safe option for advanced cancer patients who fail to respond to first-line antiemetic treatment.

Adult↗
PubMed1979

[Effect of levomepromazine on atrioventricular conduction tissue (author's transl)].

The effect of levomepromazine on sinusal automaticity, myocardial excitability and auriculoventricular conduction have been studied in dogs by measuring the spontaneous heart rate, the effective refractory period of the conduction system, the time of auriculonodal and infrahisian conduction. Chloralose-anaesthetized dogs were administered 5 mg/kg levomepromazine via IV route and 10 mg/kg one hour later. While sinusal automaticity is never altered, the other parameters studied were modified only when high doses were used. Therefore these quinidine-like effects are very unlikely to come up even following suicidal massive ingestion of levomepromazine.

Animals↗
PubMedDate not supplied

[Increased tolerance of the dopamine- and serotoninergic systems during chronic administration of haloperidol and levomepromazine].

In experiments on male albino rats single administration of haloperidol produced catalepsy, increase in dopamine turnover, enhancement of main dopamine metabolite homovanilinic acid in the forebrain. After single administration of the levomepromazine the cataleptogenic effect was accompanied by an enhanced 5-hydroxyindole acetic acid level, and no influence on the dopamine metabolism was observed. During chronic administration of haloperidol and levomepromazine their ability to induce catalepsy and to increase homovanilinic acid or 5-hydroxyindoleacetic acid concentration diminished. Thus, it appears that chronic administration of haloperidol reduces the sensitivity of dopamine receptors, and chronic administration of levomepromazine--reduces the sensitivity of dopamine and serotonin receptors in the brain.

Animals↗
PubMed1993

Citalopram: interaction studies with levomepromazine, imipramine, and lithium.

The pharmacokinetic interactions between the selective serotonin reuptake inhibitor citalopram, given as an oral dose of 40 mg/day for 10 days, and (1) levomepromazine (50 mg single oral dose), (2) imipramine (100 mg single oral dose), and (3) lithium (30 mmol/day orally for 5 days) were examined in three panels each of 8 healthy young male volunteers (age 20-31). All volunteers were classified as extensive metabolizers of sparteine and mephenytoin. Each subject completed three study phases--one with citalopram alone, one with one of the three other drugs, alone, and one with citalopram combined with the corresponding other drug. For citalopram and its metabolites, a non-enantioselective analytical method (high-performance liquid chromatography) was used. Only two statistically significant interactions were indicated. First, levomepromazine caused a 10-20% increase from the initial steady-state levels of the primary citalopram metabolite, desmethylcitalopram. Second, citalopram caused approximately 50% increase in the single-dose area under the serum concentration/time curve of desipramine (primary metabolite or imipramine) and a corresponding reduction in the level of the subsequently formed metabolite 2-hydroxydesipramine. These findings are in agreement with the recent observations that (1) the demethylation of desmethylcitalopram (to didesmethylcytalopram) is partly mediated via the sparteine/debrisoquine oxygenase (CYP2D6) and that levomepromazine is a potent inhibitor of CYP2D6, and (2) that desmethylcitalopram has a somewhat stronger affinity for CYP2D6 than desipramine, and therefore may inhibit the hydroxylation of desipramine, which is also a substrate of CYP2D6.

Adult↗